In the current work, we examined the co-expression of disease-site targeting anti-misfolded human SOD1 CARs with the co-expression of BDNF in human Tregs in both models of neuroprotection and neuroinflammation, including in a unique transgenic ALS mouse model, mSOD1-NSG mice, that expresses G93A hSOD1 transgene on an NSG genetic background, develops ALS-like disease, and does not reject injected human Tregs, so it is possible to directly test human therapeutic cells in this model [27]. Here, SOD1 is linked to amyotrophic lateral sclerosis.